Phospho-control of TGF-beta superfamily signaling
Members of the transforming growth factor-beta (TGF-beta) family control a broad range of cellular responses in metazoan organisms via autocrine, paracrine, and endocrine modes. Thus, aberrant TGF-beta signaling can play a key role in the pathogenesis of several diseases, including cancer. TGF-beta signaling pathways are activated by a short phospho-cascade, from receptor phosphorylation to the subsequent phosphorylation and activation of downstream signal transducers called R-Smads. R-Smad phosphorylation state determines Smad complex assembly/disassembly, nuclear import/export, transcriptional activity and stability, and is thus the most critical event in TGF-beta signaling. Dephosphorylation of R-Smads by specific phosphatases prevents or terminates TGF-beta signaling, highlighting the need to consider Smad (de)phosphorylation as a tightly controlled and dynamic event. This article illustrates the essential roles of reversible phosphorylation in controlling the strength and duration of TGF-beta signaling and the ensuing physiological responses.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2009 |
|---|---|
| Erschienen: |
2009 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:19 |
|---|---|
| Enthalten in: |
Cell research - 19(2009), 1 vom: 01. Jan., Seite 8-20 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Wrighton, Katharine H [VerfasserIn] |
|---|
| Links: |
|---|
| Anmerkungen: |
Date Completed 10.02.2009 Date Revised 20.10.2021 published: Print Citation Status MEDLINE |
|---|
| doi: |
10.1038/cr.2008.327 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM185478190 |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM185478190 | ||
| 003 | DE-627 | ||
| 005 | 20231223172545.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231223s2009 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1038/cr.2008.327 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n0618.xml |
| 035 | |a (DE-627)NLM185478190 | ||
| 035 | |a (NLM)19114991 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Wrighton, Katharine H |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Phospho-control of TGF-beta superfamily signaling |
| 264 | 1 | |c 2009 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 10.02.2009 | ||
| 500 | |a Date Revised 20.10.2021 | ||
| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Members of the transforming growth factor-beta (TGF-beta) family control a broad range of cellular responses in metazoan organisms via autocrine, paracrine, and endocrine modes. Thus, aberrant TGF-beta signaling can play a key role in the pathogenesis of several diseases, including cancer. TGF-beta signaling pathways are activated by a short phospho-cascade, from receptor phosphorylation to the subsequent phosphorylation and activation of downstream signal transducers called R-Smads. R-Smad phosphorylation state determines Smad complex assembly/disassembly, nuclear import/export, transcriptional activity and stability, and is thus the most critical event in TGF-beta signaling. Dephosphorylation of R-Smads by specific phosphatases prevents or terminates TGF-beta signaling, highlighting the need to consider Smad (de)phosphorylation as a tightly controlled and dynamic event. This article illustrates the essential roles of reversible phosphorylation in controlling the strength and duration of TGF-beta signaling and the ensuing physiological responses | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, N.I.H., Extramural | |
| 650 | 4 | |a Research Support, U.S. Gov't, Non-P.H.S. | |
| 650 | 4 | |a Review | |
| 650 | 7 | |a Receptors, Transforming Growth Factor beta |2 NLM | |
| 650 | 7 | |a Smad Proteins |2 NLM | |
| 650 | 7 | |a Transforming Growth Factor beta |2 NLM | |
| 650 | 7 | |a Ubiquitin |2 NLM | |
| 700 | 1 | |a Lin, Xia |e verfasserin |4 aut | |
| 700 | 1 | |a Feng, Xin-Hua |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Cell research |d 1997 |g 19(2009), 1 vom: 01. Jan., Seite 8-20 |w (DE-627)NLM09215381X |x 1748-7838 |7 nnns |
| 773 | 1 | 8 | |g volume:19 |g year:2009 |g number:1 |g day:01 |g month:01 |g pages:8-20 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1038/cr.2008.327 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 19 |j 2009 |e 1 |b 01 |c 01 |h 8-20 | ||